Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
Cancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the in...
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MDPI AG
2023-07-01
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Online Access: | https://www.mdpi.com/1467-3045/45/8/399 |
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author | Magdalena Kluska Agnieszka Wanda Piastowska-Ciesielska Paulina Tokarz |
author_facet | Magdalena Kluska Agnieszka Wanda Piastowska-Ciesielska Paulina Tokarz |
author_sort | Magdalena Kluska |
collection | DOAJ |
description | Cancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the influence of G0- and G1-arrest has not been elucidated. To study the cell cycle arrest-mediated resistance, we used MCF-7 cells and generated three populations of cells: (1) cells arrested in the G0-like phase, (2) cells that resumed the cell cycle after the G0-like phase and (3) cells arrested in early G1 with a history of G0-like arrest. We observed that both the G0-like- and the G1-arrested cells acquired resistance to apoptosis induced by oxidative stress, accompanied by a decreased intracellular reactive oxygen species and DNA damage. This effect was associated with increased autophagy, likely facilitating their survival at DNA damage insult. The cell cycle reinitiation restored a sensitivity to oxidative stress typical for cells with a non-modulated cell cycle, with a concomitant decrease in autophagy. Our results support the need for further research on the resistance of G0- and G1-arrested cancer cells to DNA-damaging agents and present autophagy as a candidate for targeting in anticancer treatment. |
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institution | Directory Open Access Journal |
issn | 1467-3037 1467-3045 |
language | English |
last_indexed | 2024-03-11T00:02:38Z |
publishDate | 2023-07-01 |
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series | Current Issues in Molecular Biology |
spelling | doaj.art-ac7c4f0111984f6cac651bb5517acab02023-11-19T00:41:39ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452023-07-014586325633810.3390/cimb45080399Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of AutophagyMagdalena Kluska0Agnieszka Wanda Piastowska-Ciesielska1Paulina Tokarz2Department of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, PolandDepartment of Cell Cultures and Genomic Analysis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, PolandDepartment of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, PolandCancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the influence of G0- and G1-arrest has not been elucidated. To study the cell cycle arrest-mediated resistance, we used MCF-7 cells and generated three populations of cells: (1) cells arrested in the G0-like phase, (2) cells that resumed the cell cycle after the G0-like phase and (3) cells arrested in early G1 with a history of G0-like arrest. We observed that both the G0-like- and the G1-arrested cells acquired resistance to apoptosis induced by oxidative stress, accompanied by a decreased intracellular reactive oxygen species and DNA damage. This effect was associated with increased autophagy, likely facilitating their survival at DNA damage insult. The cell cycle reinitiation restored a sensitivity to oxidative stress typical for cells with a non-modulated cell cycle, with a concomitant decrease in autophagy. Our results support the need for further research on the resistance of G0- and G1-arrested cancer cells to DNA-damaging agents and present autophagy as a candidate for targeting in anticancer treatment.https://www.mdpi.com/1467-3045/45/8/399autophagybreast cancercell cycleDNA damage responseoestrogenoxidative stress |
spellingShingle | Magdalena Kluska Agnieszka Wanda Piastowska-Ciesielska Paulina Tokarz Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy Current Issues in Molecular Biology autophagy breast cancer cell cycle DNA damage response oestrogen oxidative stress |
title | Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy |
title_full | Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy |
title_fullStr | Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy |
title_full_unstemmed | Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy |
title_short | Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy |
title_sort | cell cycle status influences resistance to apoptosis induced by oxidative stress in human breast cancer cells which is accompanied by modulation of autophagy |
topic | autophagy breast cancer cell cycle DNA damage response oestrogen oxidative stress |
url | https://www.mdpi.com/1467-3045/45/8/399 |
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